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BACKGROUND REPORT: VETERANS’ AFFAIRS CONSULTANCY
Justin Kenardy, PhD
March, 1998.
The amendment to the Statement of Principles for malignant neoplasm of the
prostate dated 9 December 1996 required dietary intake of 70g/day of animal fat for
at least 20 years and that should have increased by 40% associated with a period of
service in order for there to be a causal connection between that diet and the
development of carcinoma of the prostate.
In relation to this I have been asked to provide input by determining if there is
any evidence of a relationship between fat intake and addiction. In other words if fat
over-consumption can be construed as an addiction.
There are three issues I will address in covering this overall question:
1.
What are the psychological and psychophysiological processes that
facilitate fat consumption?
2.
Can fat over-consumption be viewed an addiction?
3.
Is there a special case for binge eating disorder as an example of an
addiction to food and more specifically to fat?
A number of caveats must be stated at the outset of this report.
a.
Firstly almost all research into the psychophysiology of fat
consumption does not differentiate the effects of animal from vegetable fat.
Thus no definitive statement concerning animal fat consumption and addiction
can be made.
b.
Almost all research has evaluated the effects of combined fat and
flavour, either sweet (sugar) in the majority of cases, or savoury (salt). Hence
in many instances it is not possible to absolutely distinguish the factors
associated with consumption of carbohydrates from those for fat.
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c.
In spite of this, the evidence on fat consumption can be validly considered
if one views fat consumption in relation to fat foods: foods where the macronutrient
content is primarily rather than, necessarily, exclusively fat.
1. What are the psychological and psychophysiological processes that facilitate
fat consumption?
A.
The sensory/hedonic characteristics of fat are pleasurable and reinforcing
• There are two “opponent” processes that influence food consumption, preingestive, or sensory, and post-ingestive. Afferent or sensory information
from ingested food acting in the mouth provides primarily positive
feedback for eating. The stomach and small intestine provide primarily
negative feedback to the process of consumption (Blundell & Hill, 1993).
In rats where post-ingestive process is removed (sham-feeding) the sensory
characteristics of fat alone influence intake, such that the intake of fat
increases over time (Reed, et al, 1989). Hence in terms of sensation, fat
consumption is reinforcing.
• Blundell and Hill (1993) suggest that in humans the appeal of fat lies in
the texture of fat and tastants embedded in the fat rather than the fat itself.
• However there is some evidence to suggest that there are gender
differences in the preferences for flavour-fat combinations. Pangborn, et
al. (1985) found that women’s hedonic rating of the fat in milk or chocolate
milk did not differ significantly according to fat intake or type of milk
consumed. Laurent, de Matteis, Hofstetter, and Schultz (1994) found that at
any age or weight, men preferred sweet fat food (as opposed to other fatty
or non-fatty foods.)
• Furthermore, learning may also be a factor in preference for fat. Bowen, et
al (1992) found that subjects ate more ice-cream when they were told it
was high-fat, compared with when they were told it was low-fat,
irrespective of the actual fat content, suggesting that they had learnt that
something high in fat will be more pleasurable.
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B.
The other or “opponent” side of the process of consumption of fat is the post-
ingestive effect which appears to be aversive as a means of modulating fat
consumption. This process is weakened through repeated exposure to high fat diet.
• Direct presentation of fat intragastrically is aversive (Revusky, et al, 1971;
Gonzales & Deutsch, 1985; Maggio & Koopmans, 1982).
• Rats used to a low fat diet when presented with high fat consume much less
fat than rats used to a high-fat diet (Warwick, et al, 1990).
• When rats used to a low-fat diet are put on a high-fat diet and then given a
choice of high versus low-fat foods, they consume less fat than rats who
were on a high-fat diet. (Warwick, et al, 1990)
• Although rats fed on a no-fat control diet for 12 days had higher intake of
fat-adulterated food when exposed to a choice paradigm initially, this
intake of fat decreased significantly from Day 1 to Day 3. This suggests
that although rats initially preferred the fatty food as they came off the
restricted diet (probably due to hedonic/sensory factors) this preference
very quickly decreased (probably because of aversive postingestive effects)
(Naim, et al, 1987.)
• In humans food preferences, including fat preferences, develop very early
in life and are fairly resistant to change (Capaldi, 1996).
Therefore the preference for fat, and hence increased fat intake, should be
increased in an individual if the reinforcement of the positive sensory impact of the
fat is greater than the delayed aversive postingestive consequences of consuming fat.
However the available evidence indicates that the aversiveness of post-ingestive
process appears to be intrinsic, and, furthermore, is difficult to change once
established. Similarly extended exposure to high fat can reduce the aversiveness of
the post-ingestive process. Therefore in order to change fat preferences (and
consumption), the positive sensory impact of the fat would need to be significantly
enhanced to counteract the post-ingestive negative feedback. Alternatively, the
aversiveness of the post-ingestive consequences of fat consumption would need to be
reduced through repeated exposure, although there is no data available on how long a
period this might need to be.
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C.
Information regarding the health-effects of fat can effect consumption and
preference.
Whilst there is evidence that children and adolescents are resistant to
information aimed at changing dietary preferences (Nowak & Speare, 1996; Capaldi,
1996) this is not so for adults.
• Bowen, Tomoyasu, Anderson, Carney & Kristal, (1992) found education
given about the link between diet and cancer found that it significantly
decreased consumption of, and reported preference for, fat.
• Community health-based interventions have been shown to decrease
energy from fat consumption (Sorensen, Thompson, Glanz, Feng, Kinne,
DiClemente, Emmons, Heimendinger, Probart, & Lichtenstein 1996.)
• Changes in health risk appraisal promote changes in dietary fat
consumption (Kreuter & Strecher, 1996)
Thus information can effect fat preference and consumption. The implication
being that conscious process and intention is involved in fat preference and
consumption.
D.
Three other factors have been shown to effect food preferences and
consumption, but not fat specifically.
i.
Caloric density.
• Fat is a very dense caloric food (9 kcal/g versus 4 kcal/g for protein and
carbohydrate.) Blundell and Hill (1993) suggest that due to its calorie
density a large number of “fat” calories can be consumed very rapidly
before the post-ingestive mechanisms can be brought into operation. The
overall effect is one of passive over-consumption (Blundell, Lawton,
Cotton, Macdiarmid, 1996).
• Bolles, Hayward, & Crandall (1981) also found that caloric density is more
important than number of calories in determining food preferences and
consumption.
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ii.
Emotions
 Emotions are viewed as important precursors of over-consumption of food
(Kenardy, et al, 1996.) The impact of emotions can be either to suppress
appetite (Stone & Brownell, 1994) or enhance it (Ganley, 1989).
iii.
Variation of diet
• Consumption of different foods can modify the level of satiation. For
example after eating a food to fullness, if a food of another palatable
flavour is introduced, there is a reduction of perceived fullness, and
therefore increased consumption of the more recently presented food. This
is sometimes called “the dessert effect” (Capaldi, 1996.)
2. Can fat over-consumption be view as substance dependence (or an addiction)?
If an underlying mechanism of addiction could be construed for over-consumption of
fat, it might be possible to view over-consumption of fat for an extended period of
time as due to an addiction to fat. For over-consumption of fat to be construed as an
addiction, it would need to fit within the DSM-IV (APA,1994) diagnostic criteria for
Substance Dependence. While Substance Dependence is a diagnostic category
normally reserved for alcohol and drug addiction, fat could be defined as a substance.
However there are a number of required features in order that fat over-consumption
be defined as an addiction.
A maladaptive pattern of substance use, leading to clinically
significant impairment or distress, as manifested by three (or more) of the
following, occurring at any time in the same 12-month period:
•
Tolerance, either (a) a need for a markedly increased amounts
of the substance to achieve intoxication or the desired effect, or (b) markedly
diminished effect with continued use of the same amount of the substance.
• Withdrawal, either (a) the characteristic withdrawal syndrome for
the substance, or (b) the same or closely related substance is taken to relieve
or avoid the withdrawal symptoms.
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• The substance is often taken in larger amounts or over a longer period
than was intended
• There is a persistent desire or unsuccessful efforts to cut down or control
substance use
• A great deal of time is spent in activities necessary to obtain the substance,
use the substance, or recover from its effects
• Important social, occupational, or recreational activities are given up or
reduced because of substance use
• The substance use is continued despite knowledge of having a persistent or
recurrent physical or psychological problem that is likely to have been
caused or exacerbated by the substance (APA, 1994.)
A. Tolerance.
The addiction model as applied to alcohol and psychoactive drugs explains
tolerance through a process of anticipatory conditioned compensatory responses
(CCRs). Specifically, body functions adjust to restore the homeostasis disrupted by
the substance (eg lower the core body temperature to compensate for the rise in
temperature produced by the consumption of alcohol). Through classical
conditioning the body elicits these CCRs in an anticipatory fashion when an
associated stimuli is present (eg taste, smell, environmental stimuli, even cognitions
such as thinking about drinking). These compensatory responses lower the effect of
the substance and thus increases the amount of the substance is needed to attain the
desired effect (tolerance), [or if the associated stimuli are not followed by the intake
of the substance withdrawal effects are felt.]
Jansen(1994) and others (Wilson, 1993; Woods & Brief, 1988) refer to
“cephalic phase responses” which describes conditioned compensatory responses for
eating. According to Jansen (1994) the over-consumption of carbohydrates leads to a
bodily compensatory response of releasing more insulin into the blood. This assists in
the absorption of glucose from the blood stream in order to regulate the blood-sugar
level. This process is seen as evidence of a tolerance occurring to carbohydrates.
However, there seems to be no evidence of an equivalent process for the regulation
(and thus tolerance to) fat.
• Both rats and humans (over)compensate for dilution or substitution of their
regular fat intake suggesting that there is some kind of regulatory system
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for fat. However this system is not very precise, at least in comparison to
that involved in the regulation of carbohydrate (insulin) and alcohol
(thermoregulation) consumption. For example dilution of a fat diet causes
a rebound over-consumption of up to 50% of baseline total fat intake
(Blundell & Hill, 1993; Castonguay et al., 1994; Cotton, et al, 1996).
• There is ample evidence that endogenous opioids (EO) play a role in
manipulating the consumption of fat in rats (eg Shide & Blass, 1991; Yim
& Lowy 1984). While this indicates a possible role of EOs as conditioned
compensatory responses (CCR’s) in a “fat addiction”, for EO’s to have
such a compensatory role in fat over consumption, there must be evidence
of an effect of fat consumption on the levels of EO’s (as alcohol raises
temperature, or carbohydrates increase the blood-sugar level). Only one
study could be found that provides any evidence of food consumption
effecting EO levels (Dum, Gramsch, & Hery, 1983). This study found that
the binding of an injected peptide (3H-etorphine) in the hypothalamus of
rats was significantly reduced after consumption of “highly palatable”
solution. This was interpreted for a process where the solution have
induced release of opioids. Unfortunately this highly palatable solution
was likely to be a combination of fat and sugar. There is certainly evidence
of “highly palatable” foods (rich in both fat and sugar) producing direct
effects such as high plasma Beta-endorphin levels and analgesia , and
indirect effects such as actual loss of morphine-induced analgesia (via
induced opiate tolerance through EO release) (Cohen, et al 1984; Fullerton
& Getto, 1985; Lieblich, et al 1983; McCloy & McCloy, 1979; Zhang, et
al, 1994). However there is little evidence for the effect of fat alone (as
opposed to fat combined with carbohydrates) on EOs. Thus support for a
role of EOs as compensatory mechanisms for the regulation, and thus
tolerance of fat consumption is not yet available.
B. Withdrawal
• Le Magnen (1990) reports that rats fed a “cafeteria diet” (choice of highly
palatable high energy foods) for three weeks show symptoms of
piloerection, head and whole body shaking, teeth chattering and tremors
(morphine-like withdrawal symptoms) when returned to “stock diet”
(restricted choice of lower energy food.) Although this could be construed
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as evidence of “fat withdrawal”, the “cafeteria diet” is a highly palatable,
high calorie diet, a mixture of both fat and carbohydrate. Again it is not
possible to determine whether the withdrawal effects result from fat or
high-energy carbohydrates (eg sugar.)
C. Loss of control (substance taken in larger amounts and over a longer time than was
intended)
There is no evidence from the literature that a loss of control governs fat overconsumption. While it could be argued that the tendency for over-consumption of fat
(Bludell & Hill, 1993) is an indication of fat -induced loss of control, this is most
likely due to the high caloric density and slow post-ingestive feedback of fat intake,
rather than an active over-consumption or loss of control.
Finally there is no evidence for fat over-consumption as meeting any of the
last four criteria for DSM-IV Substance Dependence. Therefore there is little support
for a “fat addiction” under the DSM-IV Substance Dependence criteria.
SUMMARY
Consumption of fat is perceived as pleasurable, however this fat preference is
1. probably related to “tastants” embedded in the fat, rather than the fat itself; 2.
subject to individual and group (gender) variation probably through associative
learning; and 3. modifiable by new information. At a psychophysiological level fat
preferences and consumption are effected by pre-ingestive sensory processes and
post-ingestive processes. It is the dynamic balance between these two processes that
determine actual consumption. Whilst it is possible to change this balance, it is
probably fairly resistant to change, requiring significantly greater sensory valance at
the pre-ingestive level, and/or a long term exposure to a new diet (eg high fat).
Overall, the evidence in favour of an addictive model of fat overconsumption is very limited and this is further supported by the “lack of fit” of
over-consumption of fat under the Substance Dependence criteria defined by
DSM-IV.
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3.
Is there special case for Binge Eating Disorder as a “fat addiction”.
Binge eating is the uncontrolled consumption of large amounts of food. As a
behaviour it can be present in anorexia nervosa, is a defining feature of bulimia
nervosa when it is also associated with compensatory behaviours such as voluntary
vomiting, and is central to a new disorder, binge eating disorder. Binge eating
disorder is included with the DSM-IV (APA, 1994) as requiring further research.
According to DSM-IV the definition of binge-eating involves two key aspects: 1.
Loss of control during eating, that is a sense that one cannot stop eating or control
what or how much one is eating; 2. Consumption of a relatively large amount of food
over a relatively short period of time (about two hours).
Furthermore according to the DSM-IV binge eating disorder must also
incorporate:
A.
Bingeing at least twice weekly for the last six months;
B.
Concern about bingeing and weight;
C.
Three of the following during most binges:
i.
Eating until feeling uncomfortably full
ii. Eating large amounts of food when not feeling hungry
iii. Eating large amounts of food throughout the day with out planned
meal time’s.
iv. Eating alone because of being embarrassed.
v.
Feeling disgusted depressed or guilty after overeating.
vi. Eating much more rapidly than usual;
D.
No compensatory behaviours (APA, 1994.)
If fat were addictive then binge eating could be viewed as an expression of
that addiction. Therefore evidence for binge eating as a special case of a “food
addiction” will be examined as well as evidence of specific fat over-consumption
within binge eating.
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Is Binge Eating Disorder possible within the population of interest?
•
Within the general population binge eating disorder is likely to be present in
about 2-4% of the population (Spitzer et al, 1992.)
•
Unlike bulimia nervosa binge eating disorder is probably comparatively
common amongst males (Spitzer et al, 1992.) Furthermore it is likely to be
present at an older age than bulimia nervosa. Finally, binge eating is closely
associated with obesity.
Is there a higher preference for fat in binge eating?
As stated above, binge eating is present in bulimia and anorexia nervosa, as
well as binge eating disorder. Within bulimia and anorexia binges are usually part of
a dietary restriction-binge cycle, whereas binges in binge eating disorder tend not that
have significant dietary restriction interposed (APA, 1994; Wilson, 1993.)
During binges associated with bulimia nervosa and anorexia nervosa evidence
indicates there is a higher consumption of fat (percentage of total calories consumed)
but that this is seen to be a function of restriction of fat (van der Ster, et al, 1994;
Kales, 1990; Tuschl et al, 1990; Woell et al, 1989.)
In contrast the limited studies of macronutrient intake during binge eating in
binge eating disorder have mixed results regarding the consumption of fat in binges
than Non-binge eating.
• Rossiter et al (1992) examined obese binge-eaters took food records
for a week. They found no difference in proportions of fat or
carbohydrate intake between binge episodes and non-binge days,
but protein and fibre intake were higher on non-binge days.
• Yanovski et al (1992) found that bingers compared to non-bingers
were instructed to eat a normal meal there was no difference in
macronutrient composition, although under both conditions the
binge eater consumed significantly more calories
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• Both studies indicate that total calorie intake is increased by, on
average, 50% in the diets of patients with binge eating disorder
versus non-patient controls.
How well does binge eating disorder fit into Substance Dependence criteria?
As with fat over-consumption, binge eating disorder can also be examined in relation
to the Substance Dependence Criteria of DSM-IV.
• Tolerance
Cephalic Phase Responses (Jansen, 1994) have been hypothesised the CCR’s
within eating disorders. However as stated previously Cephalic Phase Responses have
only been linked to carbohydrates. Furthermore a study by Karhunen, et al. (1997)
showed no stronger cephalic phase response in obese binge-eaters than obese nonbinge-eaters, after examining serum insulin, free fatty acid and plasma glucose
concentrations; and salivation, feelings of hunger and desire to eat. Bingers did,
however report a greater desire to eat during food exposure than did the non-bingers.
This suggests that binge eating may be more motivationally rather than
physiologically controlled and therefore argues against a “tolerance” process.
Furthermore overcoming tolerance in the case of binge eating disorder is
different from the addiction model of alcohol and other psychoactive drugs, in that for
these substances abstinence is required for recovery; but for binge eating the goal is to
regulate meals and macronutrient intake (Gendall, et al. 1997; Goodrick & Foreyt
1991).
•
Withdrawal
Similar arguments can be applied to withdrawal as to tolerance. For example
Jansen (1994) proposed that CCRs tend to experienced as “craving” or withdrawal
from the substance. Further, binge eating exaggerates the hypoglycaemic (craving)
response because the conditioning is stronger when the intake of the substance is
huge (rendering the body hypoglycaemic if the substance is not consumed).
•
The substance is often taken in larger amounts or over a longer period than
was intended
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The defining characteristics of binge eating are encompassed within this
criterion, that is loss of control of consumption and over-consumption.
Marcus (1993) reported that obese binge-eater (compared to obese non-binge
eaters) had significantly less perceived control over eating; and they were more
preoccupied with thoughts of food, and impulses to overeat.
•
There is a persistent desire or unsuccessful efforts to cut down or control
substance use
While there is evidence in bulimic patients that they restrict their diets in
response to episodes of binge eating, in obese binge eaters, compared to obese nonbinge eaters there is less of a tendency to apply specific strategies to control
consumption. However there is typically a long history of repeated unsuccessful
efforts to control food intake (APA, 1994)
•
There is no evidence to support binge eating disorder as meeting the last three
criteria for substance dependence.
In summary, there is some evidence that Binge Eating Disorder could be
construed as an addiction. However, the level and amount of this evidence is not
conclusive.
__________________________________________________
Is Binge Eating Disorder a possible mechanism for the Statement of
Principles Criterion for fat over-consumption as a cause of Prostate Cancer?
•
Binge Eating Disorder could possibly be considered as an addiction, but the
evidence is not conclusive.
•
If certain assumptions are made based on the literature then it could be argued that
a person who engaged in binge eating on a daily basis for 20 years would
probably exceed the 70 g animal fat consumption required for the dietary fat
intake criterion in the Statement of Principles.
•
The following assumptions are required for this conclusion to be supported:
1. That binge eating is associated with a 50% increase in total daily
calorie intake and a proportional macronutrient increase (Roster et al,
1992; Yanovski et al, 1992);
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2. In the National Dieting Survey of Australian Adults (1983) men aged
55-64 (closest to WWII veterans had a mean daily intake of 96g of fat
(55.3 g or 58% of which is animal fat).
__________________________________________________________
•
However it is also worth noting that according to Polivy et al (1994) binge eating
is rare amongst combat veterans but significantly more prevalent amongst POW’s
(European Theatre) who suffered significant weight loss. Therefore, if anything
the likelihood of binge eating of a clinical severity (ie daily for 20 years) amongst
WWII veterans would be greatly increased by dietary deprivation (caloric
restriction) rather than excess (increased fat consumption.)
___________________________________________________
In conclusion it is unlikely that Binge Eating Disorder would provide a means
for meeting the SOP Criterion on fat over-consumption.
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